METHOD: TVS of the cervix was performed before term labor induction. Induction was considered successful if vaginal delivery was achieved within 24 hours; 231 women were available for final analysis.
RESULTS: Analysis of the receiver operator characteristics curve showed an optimal cut-off for cervical length of < or = 20 mm for successful induction. Following multivariate logistic regression analysis, a sonographic short cervix (AOR 5.6; p < 0.001) was an independent predictor of successful induction but not a favorable Bishop score (p = 0.47). Among multiparas with a short cervix, positive and negative predictive values for successful induction were 98% (95% CI 90-100%) and 21% (95% CI 13%-32%) and among nulliparas, predictive values were 69% (95% CI 53%-82%) and 77% (95% CI 64%-87%) respectively.
CONCLUSION: In nulliparas, cervical length can usefully predict labor induction outcome.
METHODS: A total of 234 invasive cervical carcinomas (152 squamous cell carcinomas, 61 adenocarcinomas and 21 adenosquamous carcinomas) and 16 cervical intraepithelial neoplasia (CIN) I, six CIN II and 25 CIN III were immunohistochemically studied for p53.
RESULTS: p53 was detected more frequently in CIN and invasive carcinoma (100% of CIN I, 74.2% CIN II + III and 70.1% invasive carcinoma) compared with benign cervices (P< 0.001); however, only three squamous cell carcinomas, 11 adenocarcinomas and two adenosquamous carcinomas exhibited p53 expression in >75% of tumour nuclei. Six of the 11 adenocarcinomas and both adenosquamous carcinomas were poorly differentiated compared with one of the three squamous carcinomas. p53 immunoreactive cells were randomly distributed in invasive carcinoma, confined to the lower third of the epithelium in CIN I, reached the middle third in 20% of CIN II and upper third in 16.6% of CIN III.
CONCLUSIONS: Assuming that p53 immunoreactivity indicates gene mutation when the majority (> 75%) of neoplastic cells express p53, p53 mutations would seem uncommon in cervical carcinogenesis. Nonetheless, glandular malignancies, in particular poorly differentiated variants, may show a higher frequency of mutation. p53 was detected more frequently in CIN I compared with CIN II/III and invasive carcinoma which may be due to p53 protein degradation following interaction with high risk human papillomavirus E6 protein in CIN II/III and invasive carcinoma.